Association between neprilysin polymorphisms and sporadic Alzheimer's disease
The deposition of amyloid beta peptide (Aβ) in the form of plaques in the brain is a hallmark of Alzheimer's disease (AD). Neprilysin is the major Aβ-degradating enzyme and reduction in neprilysin activity could contribute to Alzheimer's by increasing the steady-state level of Aβ. To provi...
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| Veröffentlicht in: | Neuroscience letters 2007-11, Vol.427 (2), p.103-106 |
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| container_title | Neuroscience letters |
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| creator | Wood, Linda S. Pickering, Eve H. McHale, Duncan Dechairo, Bryan M. |
| description | The deposition of amyloid beta peptide (Aβ) in the form of plaques in the brain is a hallmark of Alzheimer's disease (AD). Neprilysin is the major Aβ-degradating enzyme and reduction in neprilysin activity could contribute to Alzheimer's by increasing the steady-state level of Aβ. To provide further evidence for the role of neprilysin in AD we genotyped 22 polymorphisms, 21 SNPs and the GT repeat in the promoter region, across the neprilysin gene in 298 Caucasian sporadic Alzheimer's patients and 298 age-matched controls. Several SNPs showed genotypic and allelic association to AD. SNP rs1836915, in linkage disequilibrium block 2, showed the greatest extent of genotypic association with AD (
p
=
0.0076). We were unable to replicate any of the SNPs that were previously reported as putatively associated with AD. However, these novel findings add to the weight of evidence supporting the involvement of neprilysin in the aetiology of Alzheimer's disease. |
| doi_str_mv | 10.1016/j.neulet.2007.09.019 |
| format | Article |
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p
=
0.0076). We were unable to replicate any of the SNPs that were previously reported as putatively associated with AD. However, these novel findings add to the weight of evidence supporting the involvement of neprilysin in the aetiology of Alzheimer's disease.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2007.09.019</identifier><identifier>PMID: 17928142</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer Disease - genetics ; Alzheimer's disease ; Biological and medical sciences ; Caucasian ; European Continental Ancestry Group - genetics ; Female ; Fundamental and applied biological sciences. Psychology ; Genotype ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Neprilysin ; Neprilysin - genetics ; Polymorphism, Single Nucleotide ; Polymorphisms ; Promoter Regions, Genetic - genetics ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2007-11, Vol.427 (2), p.103-106</ispartof><rights>2007 Elsevier Ireland Ltd</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-2eb1ad0ac2aa78bf7330982ec1166900ba911af3578f14625158b19b0cc753733</citedby><cites>FETCH-LOGICAL-c390t-2eb1ad0ac2aa78bf7330982ec1166900ba911af3578f14625158b19b0cc753733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neulet.2007.09.019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19559903$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17928142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wood, Linda S.</creatorcontrib><creatorcontrib>Pickering, Eve H.</creatorcontrib><creatorcontrib>McHale, Duncan</creatorcontrib><creatorcontrib>Dechairo, Bryan M.</creatorcontrib><title>Association between neprilysin polymorphisms and sporadic Alzheimer's disease</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>The deposition of amyloid beta peptide (Aβ) in the form of plaques in the brain is a hallmark of Alzheimer's disease (AD). Neprilysin is the major Aβ-degradating enzyme and reduction in neprilysin activity could contribute to Alzheimer's by increasing the steady-state level of Aβ. To provide further evidence for the role of neprilysin in AD we genotyped 22 polymorphisms, 21 SNPs and the GT repeat in the promoter region, across the neprilysin gene in 298 Caucasian sporadic Alzheimer's patients and 298 age-matched controls. Several SNPs showed genotypic and allelic association to AD. SNP rs1836915, in linkage disequilibrium block 2, showed the greatest extent of genotypic association with AD (
p
=
0.0076). We were unable to replicate any of the SNPs that were previously reported as putatively associated with AD. However, these novel findings add to the weight of evidence supporting the involvement of neprilysin in the aetiology of Alzheimer's disease.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer's disease</subject><subject>Biological and medical sciences</subject><subject>Caucasian</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genotype</subject><subject>Humans</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neprilysin</subject><subject>Neprilysin - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Polymorphisms</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtP3DAUha2qqAy0_wChbAqrhGvn4XiDNEJ9IFF1A2vLcW6ER4kdfDNFw6_HoxmJXVd3892jcz7GLjgUHHhzsyk8bkdcCgEgC1AFcPWJrXgrRS6VFJ_ZCkqo8lJVcMrOiDYAUPO6-sJOuVSi5ZVYsT9romCdWVzwWYfLK6LPPM7RjTtyPpvDuJtCnJ8dTZQZ32c0h2h6Z7P1-PaMbsJ4TVnvCA3hV3YymJHw2_Ges6efPx7vfucPf3_d360fclsqWHKBHTc9GCuMkW03yLIE1Qq0nDeNAuiM4twMZS3bgVeNSK3bjqsOrJV1mehzdnXInWN42SItenJkcRyNx7Al3bRVnSbyBFYH0MZAFHHQadlk4k5z0HuNeqMPGvVeowalk8b0dnnM33YT9h9PR28J-H4EDFkzDtF46-iDU3WtFOyL3h44TDb-OYyarENvsXcR7aL74P7f5B1v-5MH</recordid><startdate>20071105</startdate><enddate>20071105</enddate><creator>Wood, Linda S.</creator><creator>Pickering, Eve H.</creator><creator>McHale, Duncan</creator><creator>Dechairo, Bryan M.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20071105</creationdate><title>Association between neprilysin polymorphisms and sporadic Alzheimer's disease</title><author>Wood, Linda S. ; Pickering, Eve H. ; McHale, Duncan ; Dechairo, Bryan M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-2eb1ad0ac2aa78bf7330982ec1166900ba911af3578f14625158b19b0cc753733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer's disease</topic><topic>Biological and medical sciences</topic><topic>Caucasian</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genotype</topic><topic>Humans</topic><topic>Linkage Disequilibrium</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neprilysin</topic><topic>Neprilysin - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Polymorphisms</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wood, Linda S.</creatorcontrib><creatorcontrib>Pickering, Eve H.</creatorcontrib><creatorcontrib>McHale, Duncan</creatorcontrib><creatorcontrib>Dechairo, Bryan M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wood, Linda S.</au><au>Pickering, Eve H.</au><au>McHale, Duncan</au><au>Dechairo, Bryan M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association between neprilysin polymorphisms and sporadic Alzheimer's disease</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2007-11-05</date><risdate>2007</risdate><volume>427</volume><issue>2</issue><spage>103</spage><epage>106</epage><pages>103-106</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>The deposition of amyloid beta peptide (Aβ) in the form of plaques in the brain is a hallmark of Alzheimer's disease (AD). Neprilysin is the major Aβ-degradating enzyme and reduction in neprilysin activity could contribute to Alzheimer's by increasing the steady-state level of Aβ. To provide further evidence for the role of neprilysin in AD we genotyped 22 polymorphisms, 21 SNPs and the GT repeat in the promoter region, across the neprilysin gene in 298 Caucasian sporadic Alzheimer's patients and 298 age-matched controls. Several SNPs showed genotypic and allelic association to AD. SNP rs1836915, in linkage disequilibrium block 2, showed the greatest extent of genotypic association with AD (
p
=
0.0076). We were unable to replicate any of the SNPs that were previously reported as putatively associated with AD. However, these novel findings add to the weight of evidence supporting the involvement of neprilysin in the aetiology of Alzheimer's disease.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>17928142</pmid><doi>10.1016/j.neulet.2007.09.019</doi><tpages>4</tpages></addata></record> |
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| ispartof | Neuroscience letters, 2007-11, Vol.427 (2), p.103-106 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Aged Aged, 80 and over Alzheimer Disease - genetics Alzheimer's disease Biological and medical sciences Caucasian European Continental Ancestry Group - genetics Female Fundamental and applied biological sciences. Psychology Genotype Humans Linkage Disequilibrium Male Middle Aged Neprilysin Neprilysin - genetics Polymorphism, Single Nucleotide Polymorphisms Promoter Regions, Genetic - genetics Vertebrates: nervous system and sense organs |
| title | Association between neprilysin polymorphisms and sporadic Alzheimer's disease |
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